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Immunology Flashcards

1
Q

Granulocytes Mnemonic

A 
Never Let Mom Eat Beans
Neutrophils - 60%
Lymphocytes - 30%
Monocytes - 8%
Eosinophils - 2%
Basophils - 1 %
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2
Q

What produces IL-3 and what does it do?

A
  • Produced by activated T cells

- It stimulates growth and differentiation of stem cells in the bone marrow

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3
Q

What produces IL-4 and what does it do?

A
  • Produced by TH2- Helper T cells

- It stimulates growth of B cells and increases the number of TH2-Helper T cells at the site of inflammation

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4
Q

What produces IL-10 and what does it do?

A
  • Produced by macrophages and TH2-Helper T cells
  • It is an anti-inflammatory cytokine
  • Limits the production of Pro-inflammatory cytokines such as Interferon Gamma, IL-2, IL-3 and TNF-alpha
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5
Q

What produces INF-gamma and what does it do?

A
  • Produced by activated T cells

- Recruits leukocytes and activates phagocytosis

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6
Q

What does Leukotriene B4 do?

A
  • A metabolite of arachidonic acid, it stimulates neutrophil migration to the site of inflammation
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7
Q

Clinical features of Antiphospholipid Antibody Syndrome?

A

Venous or Arterial Thromboembolic Disease

  • Deep venous thrombosis
  • Pulmonary Embolism
  • Ischemic Stroke/Transient Ischemic Attack
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8
Q

What can happen during pregnancy in a patient Antiphospholipid Antibody Syndrome?

A
  • Unexplained embryonic or fetal loss

- Premature birth due to placental insufficiency or preeclampsia

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9
Q

What are the lab findings in Antiphospholipid Antibody Syndrome?

A 
Lupus Anticoagulant Effect
- aPTT prolongation, producing hyper coagulable state due to activation of phospholipid-dependent coagulation pathways.
Antiphospholipid antibodies
- Anticardiolipin antibody
- Anti-beta2-glycoprotein-I antibody
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10
Q

What is Antiphospholipid Antibody Syndrome?

A
  • May be primary or secondary to other autoimmune diseases such as lupus
  • Characterized by present of antiphospholipid antibodies in the setting of venous or arterial thromboembolism and/or recurrent pregnancy loss
  • Antibodies are present in 10-30% of patients with Lupus but not all exhibit the syndrome
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11
Q

What produces IL-12 and what is its effect?

A
  • Produced by macrophages

- Stimulates differentiation of T-cells into TH1- subset

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12
Q

Hapten

A
  • Less than 6000 D
  • Too small to set off an immune response
  • 90% of viruses are haptens
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13
Q

Why is it that 95% of the population has CMV and 70% of the population has EMV but they dont get mononucleosis?

A
  • Because the virus is a hapten and it is too small to set up an immune response
  • It also lacks variability to set off the immune response
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14
Q

What is the most important factor that determines immunogenicity?

A

Variability

  • It means how different a virus looks to the immune system
  • Ex Influenza virus, H1N1 is the variable factor
  • With time the virus mutates and gains variability setting off the immune system
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15
Q

Immunogen

A
  • More than 6000 D

- Large enough to set off the immune system

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16
Q

What is an antigen?

A
  • Anything that can be defined, whether it sets off the immune response or not.
  • 90% are proteins
  • Some are carbs
  • The least are lipids (cardiolipin)
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17
Q

Describe the carrier effect and how macrophages process any antigen?

A
  1. Phagocytosis
    - They ingest the antigen
  2. Phagosome formation
    - Lysosomes wrap around the object and release digestive enzymes (acid hydrolases)
  3. Digestion of the antigen
  4. Presentation
    - MHC 2 complexes present foreign antigens to T cells and B cells
    - Beta region is used to present the antigeb
  5. Displacement
    - Invariant chain is displaced
  6. IL-1 is released
    - Macrophages release IL-1 causing fever
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18
Q

What is innate immunity?

A
  • You are born with it
  • Consists of neutrophils, macrophages, monocytes, dendritic cells, NK cells and complement
  • Resistance occurs through generations
  • Response to pathogens is nonscpecific, occurs rapidly and has no memory
  • Physical barriers are the skin, epithelial tight junctions, mucus
  • Proteins secreted are lysozyme (saliva), the complement, C-reactive protein, defensins
  • Toll-like receptors recognize pathogen-associated molecular patterns (PAMPS) such as LPS (gram - bacteria), flagellin (bacteria) and nucleic acids (viruses)
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19
Q

What is acquired immunity?

A
  • You acquire it
  • Either via infection or via vaccination
  • Consists of T cells, B cells, circulating antibodies
  • Can have variation due to V(D)J recombination during lymphocyte development
  • Highly specific, refined over time, develops over long periods of time, memory response is faster and more robust
  • No physical barriers
  • Proteins secreted are immunoglobulins
  • Consists of memory cells: activated B and T cells subsequent exposure to a previously encountered antigen leads to a stronger and quicker immune response
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20
Q

Live attenuated vaccine

A
  • Vaccine is denatured so that virus can not produce infection
  • You keep the variability in order to get an antibody response
  • 1-3 % chance of people get infection
  • 10% of immunocompromised get infection
  • Do not give to immunotcompromised
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21
Q

Killed inactive vaccine

A
  • Virus is killed so it does not cause infection
  • Used for deadly viruses which you might die from
  • Rabies, polio, influenza
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22
Q

Conjugated vacccine

A
  • For bacteria
  • Means a piece of the bacteria (hapten) is attached to a immunogen
  • That way the immune system responds to the immunogen without producing infection
  • Vaccine may fail if hapten falls off immunogen or if the patient has anergy (already sick)
  • This is why vaccines are given on the same day
  • DPT (Diphtheria, Pertussis, Tetanus)
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23
Q

How do you know if a vaccine is working?

A

Check the IgG levels (memory)

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24
Q

Toxoid vaccine

A
  • For bacteria that produce a toxin
  • The toxin is what will kill the patient, not the bacteria
  • Tetanus toxin, botulinum toxin
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25
Q

Fever

A
  • One degree above normal body temperature
  • Due to IL-1 production
  • Raises HR by about 10 BPM for every 1 degree increase
  • Allows immune cells to circulate faster
  • Causes secretion of IgA in mucosal surfaces
  • Causes discomfort after about 101 degrees, treat if above
  • Fever by itself cannot tell you cause of infection
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26
Q

Macrophages in the brain

A

Microglia

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27
Q

Macrophages in the lungs

A

Alveolar macrophages

- Phagocytose foreign materials, release cytokines and alveolar proteases

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28
Q

Macrophages in the liver

A

Kupffer cells

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29
Q

Macrophages in the spleen

A

Reticuloendothelial cells

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30
Q

Macrophages in the lymph nodes

A

Dendritic cells

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31
Q

Macrophages in the bone

A

Osteoclasts

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32
Q

Macrophages in the kidneys

A

Mesangial cells

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33
Q

Macrophages in the intestines

A

M-cells in peyers patches

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34
Q

Macrophages in the skin

A

Langherhans cells

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35
Q

Macrophages in the blood

A

Monocytes

  • Emerge put of the bone marrow with CD-4 marker
  • When they enter tissue, graduate to CD-14 marker
  • Transformation allowed via interferon gamma produced by T-cells
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36
Q

Macrophages in connective tissue

A
  • Epitheloid cells
  • Giant cells
  • Histiocytes
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37
Q

Name the 8 most common T-cell immunodeficiencies

A
  1. DiGeorge Syndrome (Thymic Aplasia)
  2. Chronic mucocutaneous candidiasis
  3. Steroids
  4. Cyclosporine
  5. Hairy cell leukemia
  6. SCID
  7. Wiscott-Aldridge syndrome
  8. HIV
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38
Q

What is DiGeorge Syndrome?

A
  • Third pharyngeal pouch is missing
  • Missing thymus and imferior thyroids
  • Hypoparathyroidism
  • Has hypocalcemia, morelikely to depolarize
  • Associated with chromosome 22
  • Same chromosome as CML, Neurofibromatosis and Ewing Sarcoma
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39
Q

What 4 syndromes are associated with chromosome 22?

A
  • Digeorge
  • CML 9-22
  • Neurofibromatosis 17-22
  • Ewing sarcoma 11-22
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40
Q

What is Chronic Mucocutaneous Candidiasis?

A
  • T cell defect at sub-molecular level
  • T- cells can fight everything except candida
  • Candida infections on skin and mucous membranes
  • Chronic fatigue syndrome
  • Feel warned down, spit, pee and bowel had curdy white dischrage
  • Treat with miconazole
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41
Q

What are the anti-inflammatory actions and the physiologic actions of steroids?

A 
Anti-inflammatory actions
- Kills T cells and eosinophils
- Inhibit macrophage migration
- Stabilize mast cell membranes
- Stabilize endothelium
- Inhibit phospholipase A
Physiologic actions
- Proteolysis
- Gluconeogenesis
- Upregulates all receptors during stress
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42
Q

Prednisone

A
  • Main oral steroid
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43
Q

Hydrocortisone

A
  • Main topical or injectable form
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44
Q

Methylprednisolone

A
  • Main IV form
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45
Q

Betamethasone and Beclomethasone

A
  • Enhances surfactant production in the fetus
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46
Q

Triamcinolone

A
  • Main inhaled form

- For asthma maintenance

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47
Q

Fluticasone and Mometasone

A
  • Main spray form for nasal allergies
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48
Q

Fludrocortisone

A
  • Main replacement for aldosterone in patients with adrenal insufficiency
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49
Q

Danazole

A
  • Main treatment for endometriosis
  • Most adrogenic
  • Creates imbalance between androgens and estrogens
  • Causes endometrial tissue atrophy
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50
Q

Cypropterone

A
  • Blocks DHT receptors

- For prostate cancer

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51
Q

Megesterol

A
  • Used to increase appetite in cancer patients
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52
Q

Dexamethasone

A
  • Best CNS penetration
  • Now the DOC for increased surfactant production in premature newborns
  • Crosses the placenta faster
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53
Q

What is cyclosporine, what are its side effects and what is used now instead?

A
  • Prolongs longevity of transplanted organs
  • Inhibits calcineurin
  • Calcinuerin is needed for interleukin production
  • Side effects are gingival hyperplasia, hirsutism and renal failure at PCT
  • Tacrolimus is used now with less side effects
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54
Q

Hairy cell leukemia

A
  • Most common B cell leukemia
  • Cell have hairy cell membranes projections or fried egg appearance
  • Tartrate resistant acid phosphatase (TRAP) is the marker
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55
Q

What is more common, B or T lymphocytes?

Which is more likely?

A

You have 98 B lymphocytes for every 2 T lymphocytes
Therefore it is more common to be a B cell leukemia
Hoever the incidence of hairy Cell leukemia in T form is 25% of the general population, so its is more likely

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56
Q

How do T cell lymphomas present cutaneously and in the blood?

A
  • Mycosis fungoides in the skin, looks like fungus
  • Sezary syndrome in the blood
  • T cells have characteristic indented cell membrane
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57
Q

SCID

A
  • Autosomal recessive, 25% chance of getting
  • Adenosine deaminase deficiency
  • DNA synthesis is disrupted
  • Affects all rapidly dividing cells
  • Affects T-cells and B-cells
  • Diagnosed in fetus via chorionic villous sampling at 12 weeks
  • Bone marrow transplant done in newborn
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58
Q

Wiscott-Aldridge Syndrome

A
  • Involves T cell interaction with B cells
  • X-linked recessive
  • Carried by females, males get it
  • Fair skinned, eczema, thrombocytopenia
  • Increased incidence of lymphoma (10-12%)
  • Normal IgA and IgE
  • Problem with isotype switching back to IgM
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59
Q

What are the 4 mechanisms that can affect any type of antibody production?

A
  • Class switching does not work
  • IL-4 is defective
  • CD-40 receptor is defective
  • Tyrosine kinase is defective, second messenger
60
Q

Name the most common B-cell immunodeficiencies

A
  • Brutons agammaglobulinemia
  • CVID (Common Variable Immunodeficiency)
  • Leukemias
  • Lymphomas
  • Plasmacytoma
  • Multiple myeloma
  • Heavy chain disease
  • Selective IgA deficiency
  • Selective Ig-G2 deficiency
  • Jobs syndrome
  • SCID
  • Wiskott-Aldridge
61
Q

Brutons agammaglobulinemia

A
  • X-linked recessive (Increased in men)
  • Defect in BTK (tyrosine kinase gene)
  • Cell signaling is defective
  • B-cell count is normal but function is lacking (B cells do not mature)
  • Early onset
  • Nonsense or frameshift mutation, means the protein is defective from the beginning
  • Presents with recurrent bacterial and enteroviral infections after 6 months of age when maternal IgG is gone
  • Labs show decreased Ig of all classes
  • Absent/scanty lymph nodes and tonsils
  • Live vaccines are contraindicated
62
Q

Common Variable Immunodeficiency (CVID)

A
  • Late onset Bruton’s, after the first year of life
  • B-cell count is normal, but function is lacking (B cells do not differentiate)
  • Cell signaling is defective
  • Missense mutation, only one amino acid is off
  • Protein is functional but then stops
  • Must order a B-cell function test, exposes B cells to endotoxin or pokeweed mitogen to stimulate them and see if they will replicate
  • Tranfuse immunoglobulins when patients become septic (IVIG)
  • Increased risk for autoimmune disease, bronchiectasis, lymphoma and sinopulmonary infections
  • Labs show decreased plasma cells and decreased immunoglobulins
63
Q

What is a plasma cell?

A
  • An activated B-lymphocyte that can produce antibodies

- Has lots of Rough Endoplasmic reticulum because the antibodies they produce are proteins

64
Q

What are the two main types of plasma cell neoplasms? And what are the findings?

A
  1. Plasmacytoma
    - Only one lesion or tumor in the bone or soft tissue
  2. Multiple Myeloma
    - Multiple osteolytic lesions of plasma cells
    Ruleaux formations
    - Group of red blood cells clumped due to IgG poking them
    - Can clog up vessels
    Hypercalcemia is due to increased bone turnover
    - Due to increased osteoclastic activity
    - Can use bisphosphonates to decrease osteoclastic activity
    - IgG is the most common monoclonal spike
    - Kappa light chains are the most common Bence jones protein
65
Q

What is heavy chain disease?

A
  • IgA multiple myeloma of the bowel wall
  • IgA plasma cells are visible on biopsy
  • Causes malabsorption
66
Q

Selective IgA deficiency

A
  • Patients always get mucosal infections
  • Missing IgA
  • 95% of the time patient also has selective IgG2 deficiency
  • Patients will get anaphylaxis during blood transfusion
  • Must use a filter for subsequent transfusions or must use blood from IgA deficient patient
67
Q

Selective IgG2 deficiency

A
  • Patients always get recurrent encapsulated organism infections
  • IgG is the main opsin, it coats encapsulated organisms
  • If gram positive then it is streptococcus pneumoniae
  • If gram negative, then can be:
    Salmonella
    Klebsiella
    Hemophylus Influenza B
    Pseudomonas
    Neisseria (largest capsule)
    Citrobacter
68
Q

Jobs syndrome

A
  • Cell signaling defect
  • Increased IgE levels, problem with isotype switching or tyrosine kinase, IL-4 or CD40 ligand defects
  • Fair skinned
  • Red haired female
69
Q

What are the three neutrophil defects?

A
  1. Myeloperoxidase deficiency
  2. NADPH-Oxidase deficiency or Chronic Granulomatous Disease
  3. Absolute neutropenia
70
Q

Myeloperoxidase deficiency

A
  • Used to kill gram positives

- Recurrent gram positive infections

71
Q

NADPH Oxidase or Chronic Granulomatous Disease

A
  • X- linked recessive (1 of 5 diseases)
  • Negative Nitroblue Tetrazolium test (NBT) (Detects NADPH oxidase) does not change enzyme to blue, stays yellow
  • Get recurrent catalase positive infections
    > Staphyloccocus aureus
    > Serratia Marcescens
    > Pseudomonas
    > Nocardia
    > Aspergillus
    > Candida
    > E. coli
72
Q

Absolute Neutropenia

A
  • Neutrophils are first line of defense, show up at 4.5 hours, predominate at 24 hrs and peak at 3 days
  • Absolute Neutrophil Count = (% Neutrophils + % bands) X WBC
    < 2500 = Neutropenia
    < 1500 = Moderate
    < 1000 = Severe
  • At risk for Staph Aureus and Pseudomonas
  • Cover each with its own antibiotic (2 total)
  • This covers the humoral immunity
  • If fever persist for 48 hours, cover for fungus by adding another medication
  • This indicates that cell mediated immunity is the problem
73
Q

Which patients are at risk for Staph Aureus and Pseudomonas infections?

A
  • Absolute neutropenia patients
  • Cystic fibrosis patients
  • Burned patients
  • Diabetic patients
74
Q

What two diseases consist of macrophage defects?

A
  1. NADPH Oxydase deficiency or Chronic Granulomatous Disease

2. Chediak-Higashi Disease

75
Q

Chediak Higashi

A
  • Lysosomes are slow to fuse with ingested pathogen
  • If you want a protein to redirect to the lysosome you label it with manose 6 phosphate
  • Lysosome inclusion bodoes
  • Tyrosinase is in the lysosomes so they can not synthesizemelalin
  • Leads to albinism
76
Q

HIV

A

Highest risk are:
- Heterosexual black women (due to bisexual men)
- Elderly (they were not screened in the past)
Lowest risk:
- Prebupertal females (due to alkolic vagina)
HIV likes acidic medium, mucosa and CD-4 receptors

77
Q

Where are CD-4 receptors found?

A
  1. Female cervix
    - This is why when male ejaculates, HIV attaches to the cervix right away
    - Anytime you see advanced stages of cervical cancer, screen for HIV
  2. Blood vessels
    - When HIV attaches to vessels, they become inflammed causing vasculitis
    - Can lead to renal artery stenosis, renal failure, glomerulonephritis, papillary necrosis, interstitial nephritis, rapid progressive glomerulonephritis
    - Most common nephrotic syndrome is focal-segmental glomerulonephritis
    - Can not get membranous or membranoproliferative because there is no deposition of immune complexes
    - Blood vessels become so irritated and dysplastic that they become neoplastic
    - This is why you get kaposis sarcoma, an angiosarcoma
    - Veins are more superficial which is why kaposi sarcoma is described as violaceous nodules
  3. Macrophages
    - HIV travels in macrophages throughout the blood when it becomes phagocytosed
    - Macrophages can not kill HIV
    - This is how HIV has access to your body
  4. T-helper cells
    - Become infected and destroys
  5. CNS
    - Makes it easy for toxoplasmosis, CMV, Herpes
    - JC virus can lead to progressive multifocal leukoencephalopathy
    - Classic clue is startled myoclonus
    - The brain looks like swiss cheese
    - Can lead to lymphoma
  6. Testes
    - Leads to lymphoma
78
Q

How does HIV travel through the blood stream?

A
  • It uses macrophages
  • They phagocytize the virus but cannot kill it
  • Wherever the macrophage goes, the virus goes
79
Q

What are the three most common cancers seen with HIV?

A
  1. Cervical cancer
  2. Kaposi sarcoma
  3. CNS and testicular lymphomas
80
Q

How does HIV infect cells?

A
  • It attaches to CD-4 receptor with GP120, the attachment or arm
  • It then uses GP41 is a portal for entry of its RNA
  • Polymerase protein is used to integrate RNA into host genome
  • Reverse transcriptase is used for transcription
  • It uses P17 and P24 for assembly
81
Q

How do you prevent attachemnt of HIV infection?

A

CCR5 and CCR4

82
Q

How do you screen for HIV?

A
  1. Start with ELIZA
    - detects IgG antibodies
    - If negative repeat in 6-8 weeks, gives IgG time to develope
  2. If positive, Western Blotx
    - Western Blot detects proteins
  3. If urgent and patient insists on knowing, perform PCR, detects DNA and RNA
  4. For Newborns, perform PCR up to 18 months, because moms IgG is detectable up until then, if you perform ELIZA, that corresponds to moms IgG, baby begins to secrete IgG at 6 months
83
Q

T-Helper Cell counts (CD4)

A 
Normal
- Adults: 800-1200
- Newborns: 1500
Begin treatment when they fall to:
- Adults: < 350
- Peds: < 750 or 50%
Begin Pneumocystis Jiroveci Prophylaxis
- Adults < 200
- Peds < 300 or 20%
AIDS when count drops < 200
84
Q

How does Pneumocystic Jiroveci affect HIV patients?

A
  • Yeast like fungus
  • Infects the lungs
  • Goes into the interstitium
  • Causes diffusion problem
  • Patient has trouble breathing in
  • Will cause restrictive lung disease
  • Low PO2
  • Increased respiratory rate
  • Decreased PCO2
  • pH will be increased, alkalosis
  • Hypoxia will cause pulmonary vessel constriction
  • Pulmonary resistance will rise
  • Pulmonary blood flow witll decrease
  • Pulmonary capillary wedge pressure will decrease
  • S2 splitting will narrow due to resistance
  • Will create resistance problem
  • S2 will be louder
  • Higher pulmonary resistance will cause atrophy of right ventricle
  • Increased cardiac contractility
  • Diastolic dysfunction
  • Will develop S4 louder with inhalation
  • Cor pulmonal will be cause of death
85
Q

When should you begin HAART and Mycobacterium avium intracellular prophylaxis?

A

CD4 count:
Adults < 100
Pediatrics < 10%

86
Q

What are the basic guidelines for HIV treatment?

A

Start with 2 Nucleoside Inhibitors + 1 Protease Inhibitor

  • AZT
  • 3TC
  • 4DT
  • DDI or DDC
  • Rotonavir, Indinavir, Sequinavir
87
Q

How do you treat or prevent Pneumycistis Jiroveci?

A

Trimethoprim/Sulfamethoxazole

  • MOA: Trimethoprim blocks dihydrofolate reductase and Sulfamethoxazole blocks Para-Amino Benzoic Acid
  • Add leucovorin (folinic acid) to prevent megaloblastic anemia, it replaces THF
88
Q

Type 1 hypersensitivity

A
  • Anaphylactic (fast) and Atopic
  • Involves mast cells and eosinophils
  • Free antigen cross links IgE
  • Initially mast cells release:
    > Histamine, causes initial symptoms
    > Slow Reacting Substance of Anaphylaxis (SRS-A), 4-8 hrs later
    > Eosinophil Chemotactic Factor of Anaphylaxis
  • In delayed phase, eosinophils release:
    > Heparin, prevents clot formation with all of the vasodilation from histamine
    > Arylsulfatase, counteracts SRS-A
    > Histaminase, counteracts histamine
    Examples:
    Anaphylaxis (food, drug, bee sting)
    Urticaria
    Stevens-Johnson syndrome
    Erythema Multiforme
89
Q

Type 2 Hypersensitivity

A
  • Cytotoxic
  • A deliberate attack on itself
  • Complement comes in after the attack
  • Antibodies bind to cell surface antigens
  • Leads to either:
    1. Cellular Destruction
  • Cell is opsonized by antibodies leading to phagocytosis and/or activation of the complement or NK cell killing
    Examples
    Autoimmune Hemolytic Anemia
    Immune Thrombocytopenic Purpura
    Transfusion Reactions
    Hemolytic Disease of the Newborn
    2. Inflammation
  • Activation of complement system and Fc receptor mediated inflammation
    Examples
    Goodpasteur Syndrome
    Rheumatic Fever
    Hyperacute Transplant Rejection
    3. Cell dysfunction
  • Antibodies bind to cell surface receptors
  • Abnormal blockade or activation of downstream process
    Examples
    Myasthenia Gravis
    Graves Disease
90
Q

What do the direct and indirect Coombs test detect?

A
  1. Direct
    - Detects antibodies attached directly to RBC surface
  2. Indirect
    - Detects presence of unbound antibodies in the serum
91
Q

Type 3 Hypersensitivity

A
  • Immune Complex Deposition
  • Not a deliberate attack on tissue
  • Tissue is damaged due to the inflammatory response
  • So much complement is used that it is low on blood
    Examples
    SLE
    Rheumatoid Arthritis
    Cryglobulinemia
    Serum Sickness
    Post-streptococcal glomerulonephritis
92
Q

What is serum sickness?

A
  • Immune complex disease which antibodies to foreign proteins are produced
  • Takes 5 days.
  • Immune complexes form and are deposited in membranes where they fix complement.
  • Leads to tissue damage
  • More common than arthus reaction
    Most is caused by drugs now, act as haptens
  • Fever, urticaria, arthralgia, proteinuria, lymphadenopathy (5-10 days later)
93
Q

What is arthus reaction?

A
  • Local subacute antibody mediated hypersensitivity reaction
  • Intradermal injection of antigen into a presensitized (has circulating IgG) individual leads to immune complex formation in the skin
  • Characterized by edema, necrosis and activation of complement
94
Q

Type 4 Hypersensitivity

A
  • There are two mechanisms, both involve T-cells
    1. Direct cell cytotoxicity
  • CD8+ cytotoxic T cells kill targeted cells
    Example
    Type 1 diabetes mellitus
    2. Delayed-type hypersensitivity
  • Sensitized CD4+ helper T cells encounter antigen and release cytokines
  • Inflammation and macrophage activation
    Examples:
    Contact dermatitis (poison IV, nickel allergy)
    Graft vs Host disease
    TB test
95
Q

What is the main function of the complement system?

A 
To kill encapsulated organisms
Gram +
Streptococcus Pneumonia
Gram -
Salmonella
Klebsiella
Hemophylus Influenza
Pseudomonas
Neisseria
Citrobacter
96
Q

What activates the Classic, Alternative and Lectin pathways of the complement?

A

Classic: IgG or IgM
Alternative: microbe surface molecules, usually encapsulated bacteria
Lectin: Mannose or other sugars on microbes

97
Q

What is the structure of C1 and what are the functions of its proteins?

A

C1 has quaternary structure

  • C1q is a platform protein
  • C1 esterase is the enzyme cutting
  • C1 esterase inhibitor blocks the esterase from cutting when it is done
98
Q

Describe the classic pathway for complement?

A
  1. C1 cuts C4 into C4a and C4b
  2. C1 cuts C2 into C2a and C2b
  3. Keep C2b and C4b
  4. Combine them to from C4b2b (C3 convertase)
  5. C3 convertase cuts C3 into C3a and C3b
  6. Keep C3b
  7. Combine C3b and C3 convertase to make C4b2b3b (C5 convertase)
  8. C5 convertase splits C5 into C5a and C5b
  9. C5b joins C6-9 to form MAC
  10. MAC causes cell lysis and toxicity
99
Q

What is a function of C3b?

A
  • Only member that can act in opsonization
  • Binds bacteria
  • Activates neutrophils and macrophages to phagocytize bacteria
100
Q

What are functions of C3a, C4a and C5a?

A

Anaphylaxis

101
Q

What is the function of C5a?

A
  • Neutrophil chemotaxis
  • If too much is produced, can lead to angioedema
  • Recurrent facial swelling
  • Primary disease is inherited, autosomal recessive due to C1 esterase inhibitor deficiency
  • Secondary disease is caused ny ACE inhibitors and ARBs
102
Q

What is the function of C5b-C9?

A
  • MAC

- Cytolysis of cells

103
Q

Anti-Scl-70 (Anti-DNA topoisomerase I)

A

Scleroderma (Diffuse)

104
Q

MPO-ANCA/p-ANCA

A
  • Microscopic Polyangitis (form of PAN)
  • Eosinophilic Granulomatosis with Polyangiitis (Churh-Strauss syndrome)
  • Ulcerative colitis
105
Q

PR3-ANCA/c-ANCA

A

Granulomatosis with Polyangiitis (Wegener)

106
Q

Anti-Glomerular Basement Membrane

A

Goodpasteur Syndrome

107
Q

Anti- Anchoring Proteins

A

Bullous Pemphigous

108
Q

Antiplatelet

A

Idiopathic Thromocytopenic Purpura

109
Q

Anti-RBC

A

Autoimmune Hemolytic Anemia

110
Q

Antimicrosomal
Antithyroglobulin
Anti-thyroid peroxidase

A

Hashimoto Thyroiditis

111
Q

Anti-TSH receptor

A

Graves Disease

112
Q

Anti-ACH receptor

A

Myasthenia Gravis

113
Q

Anti-Myelin

A

Multiple Sclerosis

114
Q

Antiparietal Cell

Anti-Intrinsic Factor

A

Pernicious Anemia

115
Q

Antimitochondrial

A

Primary Biliary Cirrhosis

116
Q

Anti-Melanocyte

A

Vitiligo

117
Q 
Rheumatoid Factor ( IgM antibody against IgG Fc region)
Anti-CCP (more specific)
A

Rheumatoid Arthritis

118
Q

Anti-SSA (Anti-Ro)

Anti-SSB (Anti-La)

A

Sjögren Syndrome

119
Q

Anti-dsDNA
Anti-Smith
Anti-histone

A
  • Systemic Lupus Erythematosus

- Drug-Induced Lupus

120
Q

Anticardiolipin

Lupus anticoagulant

A
  • Systemic Lupus Erythematosus

- Antiphospholipid Syndrome

121
Q

Anti-Centromere

A

Limited Scleroderma (CREST Syndrome)

122
Q

Anti-smooth muscle

A
  • Autoimmune Hepatitis type 1

- Scleroderma

123
Q

Anti-U1 RNP (Ribonucleoprotein)

A

Mixed connective tissue disease

124
Q

Antinuclear (ANA)

A
  • Nonspecific screening antibody

- Often associated with SLE

125
Q

Anti-desmoglein (anti-desmosome)

A

Pemphigus Vulgaris

126
Q

Anti-Beta2 Glycoprotein

A

Antiphospholipid Syndrome

127
Q

Anti-Glutamic Acid Decarboxylase

Islet Cell Cytoplasmic Antibodies

A

Type 1 Diabetes Mellitus

128
Q

Anti-hemidesmosome

A

Bullous Pemphigoid

129
Q

Anti-synthetase (Anti-Jo-1)
Anti-SRP
Anti-helicase

A

Polymyositis

Dermatomyositis

130
Q

Antiphospholipase A2 Receptor

A

Primary Membranous Nephropathy

Membranous Glomerulonephritis

131
Q

Anti-presynaptic Voltage Gated Calcium Channel

A

Lambert-Eaton Myasthenic Syndrome

132
Q

IgA Anti-Endomysial

IgA anti-tissue transglutaminase

A

Celiac Disease

133
Q

Hyperacute Transplant Rejection

A
  • Occurs minutes to hours
  • Preformed antibodies against graft in recipients circulation
  • Morphology shows gross mottling, cyanosis, arterial fibrinoid necrosis and capillary thrombotic occlusion
134
Q

Acute Transplant Rejection

A
  • Occurs within 6 months
  • Exposure to donors antigens induces humoral/cellular activation of naive immune cells
  • Humoral: CD4 deposition, neutrophilic infiltrate, necrotizing vasculitis
  • Cellular: Lymphocytic interstitial infiltrate and endotheliitis
135
Q

Chronic Transplant Rejection

A
  • Occurs months to years
  • Chronic low grade immune response is refractory to immunosuppressants
  • Morphology shows vascular wall thickening and luminal narrowing, there is interstitial fibrosis and parenchymal atrophy
136
Q

Graft Vs Host Disease

A
  • Grafted T cells proliferate in immunocompromised host and reject host cells with foreign proteins
  • Leads to severe organ dysfunction
  • Type IV Hypersensitivity reaction
  • Usually with bone marrow and liver transplants because they are rich in lymphocytes
  • Potentially beneficial in bone marrow transplant for leukemia (graft vs tumor effect)
137
Q

What are the 4 graft types?

A

Autograft: from self
Syngeneic graft (isograft): From twin or clone
Allograft: From nonidentical same species
Xenograft: From different species

138
Q

Lymph Node Paracortex Properties

A
  • Region populated by T lymphocytes and Dendritic cells
  • Internal to the cortex between follicles and medulla
  • Dendritic cells present antigens to T lymphocytes here
  • Region becomes enlarged by proliferation of T lymphocytes during adaptive cellular immune responses
  • In DiGeorge Syndrome, region is poorly developed due to deficient mature T lymphocytes
139
Q

Lymph Node Follicle Properties

A
  • Located on the outer cortex
  • Sites of B Lymphocyte localization and proliferation
  • Primary follicles are dense and dormant
  • Secondary follicles have pale germinal center containing proliferating B cells and follicular dendritic cells
  • In Agammaglobulinemia the germinal centers and primary lymphoid follicles do not form due to absence of B cells
140
Q

Class II MHC peptides

A

Displayed only by antigen presenting cells

  • Used to present antigens that antigen presenting cells (dendritic cells, macrophages and B-lymphocytes) pick up via endocytosis or phagocytosis
  • They are degraded by acidification with endosome-lysosome fusion or phagosome lysosome fusion.
  • It is synthesized in RER and routed to the endosomes by the Golgi
  • Each molecule has a peptide fragment called an invariant chain bound to its antigen binding site
  • The fragment guides the molecule during sorting in the Golgi and occupies the site until until it enters an acidified endosome where it can bind a foreign protein.
  • Fusion of the vesicles containing MHC class II with the acidified phagolysosomes containing foreign lysosome leads to degradation of the invariant chain and loading of antigen onto MHC class II molecule
  • The MHC class II molecule-protein antigen complexes are then displayed on the surface of antigen presenting cells where they are available o bind T-cell receptors on T lymphocytes and initiate a T-cell response to the antigen they display
  • Without lysosomal acidification, antigen processing in association with MHC class II antigens would not occur
141
Q

What is Calcineurin?

How can it be inhibited?

A
  • Essential protein in the activation of IL-2
  • It promotes the growth and differentiation of T cells
  • Cyclosporine and Tacrolimus inhibit its activation
142
Q

Anaphylactic and atopy is a?

A

Type I hypersensitivity

143
Q

Antibody-dependent cellular toxicity is a?

A

Type II hypersensitivity

144
Q

Serum sickness and Arthus reaction are?

A

Type III hypersensitivities

145
Q

Delayed type hypersensitivity is a?

A

Type IV hypersensitivity

STEP (28 decks)

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